Abstract
Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the main triggers of drug hypersensitivity, probably due to their high consume worldwide, with NSAIDs-induced acute urticaria/angioedema (NIUA) being the most frequent clinical phenotype. Nevertheless, most studies have focused on NSAIDs-exacerbated respiratory disease. NSAID-hypersensitivity occurs only in some individuals, mainly by the increased release of cysteinyl-leukotrienes from arachidonic acid due to COX-1 inhibition. Thus, individual susceptibility to NSAID-hypersensitivity may be under the influence of genetic factors.
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